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<p>Ovarian hyperstimulation syndrome (OHSS) is the most severe complication of ovarian stimulation during assisted reproductive procedures and resembles an acute inflammatory response. Curcumin possesses antioxidant, anti-inflammatory, and anti-angiogenic properties. However, its impact on OHSS remains unclear. This study aimed to investigate the protective effects of curcumin in a rat model of OHSS and elucidate its underlying mechanisms. A rat model of OHSS was established using gonadotropin and human chorionic gonadotropin (hCG), followed by 7&#xa0;days of curcumin administration. Pathological changes in ovarian tissue were assessed via hematoxylin and eosin (H&amp;E) staining. The expression levels of serum estradiol (E<sub>2</sub>), vascular endothelial growth factor (VEGF), VEGF-receptor 2 (VEGFR2), and inflammatory factors were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were assessed using commercial kits. Finally, nuclear factor kappa B (NF-κB) and hypoxia-inducible factor 1-alpha (HIF-1α) levels in ovarian tissue were analyzed using western blotting. The results showed that curcumin significantly alleviated ovarian tissue pathological damage in rats with OHSS and reduced the serum levels of E<sub>2</sub>, VEGF, VEGFR2, interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). Additionally, SOD and GSH-Px levels were significantly elevated, while MDA levels were significantly diminished. Moreover, curcumin significantly inhibited NF-κB activation, downregulated HIF-1α expression, and consequently reduced VEGF expression. In summary, curcumin reduced VEGF levels by inhibiting the NF-κB/HIF-1α signaling pathway, thereby&#xa0;alleviating symptoms of gonadotropin-induced OHSS. It may serve as a potential therapeutic agent for OHSS prevention and treatment.</p>

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Curcumin alleviates ovarian hyperstimulation syndrome in the rat model via inhibiting the nuclear factor kappa B/hypoxia-inducible factor-1α signaling pathway

  • 期刊论文

  • 发表日期：

    2025年7月12日

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  • Lilan Sun,
  • Xiumei Zhuo,
  • Dandan Qi,
  • Hao Ma,
  • Fanhua Kong,
  • Pingping Sun,
  • Yan Zhang,
  • Peng Xue,
  • Huagang Ma

摘要

Ovarian hyperstimulation syndrome (OHSS) is the most severe complication of ovarian stimulation during assisted reproductive procedures and resembles an acute inflammatory response. Curcumin possesses antioxidant, anti-inflammatory, and anti-angiogenic properties. However, its impact on OHSS remains unclear. This study aimed to investigate the protective effects of curcumin in a rat model of OHSS and elucidate its underlying mechanisms. A rat model of OHSS was established using gonadotropin and human chorionic gonadotropin (hCG), followed by 7 days of curcumin administration. Pathological changes in ovarian tissue were assessed via hematoxylin and eosin (H&E) staining. The expression levels of serum estradiol (E2), vascular endothelial growth factor (VEGF), VEGF-receptor 2 (VEGFR2), and inflammatory factors were measured using enzyme-linked immunosorbent assay (ELISA). Additionally, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) levels were assessed using commercial kits. Finally, nuclear factor kappa B (NF-κB) and hypoxia-inducible factor 1-alpha (HIF-1α) levels in ovarian tissue were analyzed using western blotting. The results showed that curcumin significantly alleviated ovarian tissue pathological damage in rats with OHSS and reduced the serum levels of E2, VEGF, VEGFR2, interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α). Additionally, SOD and GSH-Px levels were significantly elevated, while MDA levels were significantly diminished. Moreover, curcumin significantly inhibited NF-κB activation, downregulated HIF-1α expression, and consequently reduced VEGF expression. In summary, curcumin reduced VEGF levels by inhibiting the NF-κB/HIF-1α signaling pathway, thereby alleviating symptoms of gonadotropin-induced OHSS. It may serve as a potential therapeutic agent for OHSS prevention and treatment.